Phenotypic and Genetic Overlap Between Autistic Traits at the Extremes of the General Population

Ronald, Angelica; Happé, Francesca; Price, Thomas S.; Baron‐Cohen, Simon; Plomin, Robert

doi:10.1097/01.chi.0000230165.54117.41

Cited by 193 publications

(178 citation statements)

References 27 publications

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“…Previous results (9)(10)(11)30) and the present study concur in suggesting that there are a degree of overlapping genetic and environmental influences between different autism behaviors in the general population but also significant genetic and environmental influences that are specific to each part of the autism triad. One slight difference is that while the results from the UK twin studies found that SIs and RRBIs showed the least amount of phenotypic and genetic overlap within the triad, the present study found that this overlap was highest between SIs and RRBIs.…”

Section: Discussionsupporting

confidence: 77%

“…These previous twin studies have reported modest to moderate genetic overlap across different parts of the autistic triad in the general population (9), in extremescoring groups (10), and in children with suspected ASDs based on a parent interview (11,12). These findings suggest that while some genetic influences may confer risk for developing all the symptoms of the autistic triad, others are specific to particular symptoms.…”

mentioning

confidence: 81%

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A twin study of autism symptoms in Sweden

et al. 2010

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Section: Discussionsupporting

confidence: 77%

mentioning

confidence: 81%

A twin study of autism symptoms in Sweden

et al. 2010

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“…12 Previous twin studies have suggested that the polygenic factors responsible for ASDs may also be responsible for more common social impairments in the general population, the severity of which falls below the threshold for categorical ASD diagnosis. 19,20 Moreover, autosomal recessive genes responsible for autism have been identified by homozygosity mapping in consanguineous pedigrees. 21 The risks from polygenic or recessive genetic factors is included in an intermediate risk class.…”

Section: Major Contribution Of Dominant Inheritance To Asds T Nishiyamentioning

confidence: 99%

Major contribution of dominant inheritance to autism spectrum disorders (ASDs) in population-based families

Nishiyama

Notohara

Sumi³

et al. 2009

J Hum Genet

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Results of twin studies have shown that autism spectrum disorders (ASDs) are attributable to complex multigenic interactions rather than to a single susceptibility gene. However, the growing number of distinct, individually rare genetic causes of ASDs, mostly copy number variations (CNVs), favors an alternative to the polygenic hypothesis, the two-component model, which suggests that ASDs are caused either by de novo mutation or by dominant inheritance from asymptomatic carriers of such a mutation. To verify this hypothesis, we estimated the distribution of ASD-risk among both catchment area-based families and multiplex families. Our results suggest that the models with more than three risk components are preferable to the twocomponent model. Our results also suggest that the largest proportion of ASD cases is caused by dominant inheritance. We additionally show that Supplementary information regarding prevalence has a crucial role in analyzing proband-ascertained data.

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“…Interestingly, the three PDD symptom domains have been suggested to originate from distinct genetic influences in both general population samples (Ronald et al 2006a, Ronald et al 2005, Ronald et al 2006b) and clinical samples (Georgiades et al 2007, Kolevzon et al 2004, although the opposite has been found as well (Dyck et al 2006, Goin-Kochel et al 2008. Thus far, the potential differential heritablility of the PDD dimensions in the context of ADHD has not been investigated.…”

Section: Introductionmentioning

confidence: 99%

PDD Symptoms in ADHD, an Independent Familial Trait?

Nijmeijer

Hoekstra

Minderaa

et al. 2008

J Abnorm Child Psychol

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The aims of this study were to investigate whether subtle PDD symptoms in the context of ADHD are transmitted in families independent of ADHD, and whether PDD symptom familiality is influenced by gender and age. The sample consisted of 256 sibling pairs with at least one child with ADHD and 147 healthy controls, aged 5-19 years. Children who fulfilled criteria for autistic disorder were excluded. The Children's Social Behavior Questionnaire (CSBQ) was used to assess PDD symptoms. Probands, siblings, and controls were compared using analyses of variance. Sibling correlations were calculated for CSBQ scores after controlling for IQ, ADHD, and comorbid anxiety. In addition, we calculated cross-sibling cross-trait correlations. Both children with ADHD and their siblings had higher PDD levels than healthy controls. The sibling correlation was 0.28 for the CSBQ total scale, with the CSBQ stereotyped behavior subscale showing the strongest sibling correlation (r=0.35). Sibling correlations remained similar in strength after controlling for IQ and ADHD, and were not confounded by comorbid anxiety. Sibling correlations were higher in female than in male probands. The social subscale showed stronger sibling correlations in elder than in younger sibling pairs. Crosssibling cross-trait correlations for PDD and ADHD were weak and not-significant. The results confirm that children with ADHD have high levels of PDD symptoms, and further suggest that the familiality of subtle PDD symptoms in the context of ADHD is largely independent from ADHD familiality.

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Phenotypic and Genetic Overlap Between Autistic Traits at the Extremes of the General Population

Cited by 193 publications

References 27 publications

A twin study of autism symptoms in Sweden

A twin study of autism symptoms in Sweden

Major contribution of dominant inheritance to autism spectrum disorders (ASDs) in population-based families

PDD Symptoms in ADHD, an Independent Familial Trait?

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